Study finds human body lice can transmit plague bacteria

By Dr. Sushama R. Chaphalkar, PhD.Reviewed by Benedette Cuffari, M.Sc.May 26 2024

In a recent study published in the journal PLOS Biology, researchers adapt a strain of human body lice to a membrane feeder to study its infection dynamics with Yersinia pestis, the causative agent of the plague.

Study: Yersinia pestis can infect the Pawlowsky glands of human body lice and be transmitted by louse bite. Image Credit: PPK_studio / Shutterstock.com

Can lice be infected with Y. pestis?

Human body lice, otherwise known as Pediculus humanus humanus, are blood-feeding parasites that thrive in conditions of poor hygiene. They are known vectors for pathogens like Bartonella quintana, Borrelia recurrentis, and Rickettsia prowazekii; however, their role in transmitting Y. pestis is controversial.

Although traditionally implicated fleas and rats are well-established vectors, recent studies suggest that human lice may also potentially transmit plague and, as a result, may have been involved in previous pandemics, including the Black Plague.

Experimental evidence shows that lice can become infected with Y. pestis, especially at high bacteremia levels, and transmit the bacterium; however, their efficiency and survival rates post-infection are variable. Previous experiments have reported low transmission rates, whereas more recent studies using rabbit-adapted lice showed higher transmission but rapid louse mortality.

Thus, further research is needed to clarify the role of body lice in plague transmission, including minimum infective doses, infection duration, and transmission mechanisms. To address this gap, researchers in the present study employed a standardized membrane feeder-adapted body louse model to evaluate the vector competence of lice for Y. pestis.

About the study

The San Francisco strain of human body louse was used in the study. Direct and delayed transfer were both used to investigate body louse vector competence for Y. pestis. Lice infection rates, mortality, bacterial transmission, and fecal shedding were monitored for one week.

Engineered strains of Y. pestis, Y. pseudotuberculosis, or Escherichia coli strains expressing mCherry were isolated on blood agar plates and cultured in brain-heart infusion broth. Fluorescence microscopy and immunohistochemistry (IHC) were used to investigate the colonization sites of Y. pestis in body lice and underlying transmission mechanisms.

The transmission efficacies of the bacterium with different feeding periods ranging from three to 20 hours were determined and compared in Pawlowsky gland (PG)-infected and midgut-only infected lice. Varying infectious blood doses ranging from 10⁴ to 10⁷ colony-forming units (CFUs)/ml were used to simulate human bacteremia for analysis.

The minimum bacteremia level required for chronic infection in body lice and PG colonization was determined. The infectivity and transmission potential of various bacterial strains, including Y. pestis and E. coli, were also examined in human body lice.

Study findings

The delayed transfer group showed higher but non-significant infection rates, mortality, and transmission rates. Both scenarios demonstrated that body lice could become chronically infected and effectively transmit Y. pestis, with their transmission efficiency remaining stable or improving by the seventh day despite Y. pestis-induced mortality.

Three localization patterns of Y. pestis were observed in the lice: no detectable bacteria, bacteria only in the midgut, and bacteria in the head with or without midgut presence. About 14% of infected lice developed head infections in PGs, with these structures speculated to assist in mouthpart lubrication. Y. pestis was found in PGs and their ducts through IHC, thus supporting their role in transmitting the bacteria.

Only lice with PG infections transmitted Y. pestis during the three-hour feeding period, with a median of 68 CFU recovered. Comparatively, during the 20-hour feeding assays, PG-infected lice consistently transmitted higher CFUs with a median of 2,000 CFU/louse compared to midgut-only lice.

Post-assay, all PG-infected lice remained infected, as compared to only 75% of midgut-only lice. Y. pestis was found in the heads of all PG-infected lice, thus indicating that PG infection enhances transmission efficiency.

A minimum bacteremia level of 1.2 x 10⁵ CFU/ml was required for Y. pestis to reliably cause chronic infection in body lice with subsequent PG colonization. While chronic infection was observed at a rate of 58% at 10⁸ CFU/ml, PG infection, and transmission occurred at bacteremia levels above or equal to 10⁷ CFU/ml. Fecal transmission potential was observed even at low bacteremia.

Chronic infection of the body louse midgut occurred within a range commonly noted in clinical case reports, whereas PG infection occurred at the upper range of human plague bacteremia. However, all tested bacterial strains could colonize body lice midguts; only Yersinia spp. could infect PGs. Infection and transmission rates were comparable among all bacterial strains.

Conclusions

The current study provides strong evidence supporting the role of human body lice as potential vectors for plague transmission. With their larger blood intake, frequent feeding, and lack of key immunity genes, human body lice are efficiently infected by and transmit Y. pestis.

Historical outbreaks, which correlate with peak rodent flea activity, indicate that body lice may have contributed significantly to the transmission of the plague under specific conditions. Thus, the study findings emphasize the importance of considering multiple vectors in formulating disease control strategies.